UK Parkinson's Disease Consortium - UKPDC
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The new Leonard Wolfson Experimental Neurology Centre (LWENC) has opened for clinical studies and trials
In this paper Claudia Manzoni studies how fibroblast
cells from people with Parkinson’s disease caused by mutations in LRRK2
react to starvation. Although the changes are quite subtle, there are
differences between the way that fibroblasts that contain mutant LRRK2
respond to being starved – suggesting that there may be changes in the
way that these cells regulate a key process called autophagy (a term
which comes from the greek meaning to eat yourself, and is one of the
ways that cells get rid of waste and recycle proteins and organellles).
Research led by consortium researchers Dr Helene Plun-Favreau (UCL Institute of Neurology) and Dr Alex Whitworth (University of Sheffield), and collaborator Dr Heike Laman (University of Cambridge), has discovered how genetic mutations linked to Parkinson’s disease might play a key role in the death of brain cells, potentially paving the way for the development of more effective drug treatments. In the new study, published in Nature Neuroscience, the team of cross-institutional researchers showed how defects in the Parkinson’s gene Fbxo7 cause problems with mitophagy. More...
Mutations in LRRK2 are the most common genetic cause of Parkinson’s disease. Here, Claudia Manzoni talks about her research (funded by the Rosetrees Trust and the Michael J. Fox Foundation) into what LRRK2 might be doing within the cell: Parkinson’s disease is a brain illness that afflicts 1 in 500 people in the UK. High profile patients, such as the actor Michael J Fox, the boxer Muhammad Ali and the late Pope John Paul II, have raised public awareness of Parkinson’s and its devastating impact. More...
Dr Laura Osellame tells us about her recent paper in Cell Metabolism about Mitochondrial dysfunction linked to loss of an enzyme called GBA: Gaucher Disease (GD) is a rare inherited disease, belonging to the family of lysosomal storage disorders. Mutations in the gene glucocerebrosidase (GBA) are responsible for the disease and can increase susceptibility to Parkinson’s disease (PD). Genetic studies undertaken at UCL and other hospitals around the world suggest that mutations in GBA are the most common genetic risk factor currently known for PD. More...
(MJFF Research Fellow)
I graduated in Pharmaceutical Biotechnology at the University of Milan and, to obtain my degree, I worked at the Mario Negri Institute for Pharmacological Research for 18 months on a project concerning the description of the synthetic peptide PrP82-146 as an in vitro model for prion amyloid. After graduation I remained at the Mario Negri Institute as research fellow in the lab. of Protein Chemistry and Biochemistry. In January 2006 I started my PhD with the Open University and I graduated in April 2010. For my PhD project I worked with Abeta amyloid investigating Abeta-induced neuronal toxicity and confirming that Abeta peptides, when appropriately folded, can impair neuronal viability following protein-mediated “docking” onto cell membranes. The aim of my study was to identify membrane proteins which might have a role in triggering Abeta-induced toxicity after binding to Abeta oligomers. In March 2010 I joined the Department of Molecular Neuroscience as associate research fellow under the supervision of Dr Patrick Lewis working on a project concerning the characterization of fibroblasts from PD patients with mutations in the LRRK2 protein, with specific interest for the mTOR and the TNFa signalling pathways.
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Page last modified on 13 aug 13 12:38